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Cardiac tamponade occurs when fluid or blood accumulates in the pericardium at a rate that does not allow adequate filling of the ventricles resulting in diminished cardiac output and shock. Symptoms include shortness of breath, orthopnea, dyspnea on exertion, syncope, and symptoms of inadequate perfusion. Hypotension, tachycardia, pulsus paradoxus, and JVD are examination findings seen in tamponade. Causes include blunt or penetrating trauma, malignancy, hypothyroidism, uremia, myocardial or aortic rupture, and pericarditis. Rapid filling of the pericardial sac (50-100 mL) is more likely to cause cardiovascular compromise than gradual accumulation.
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Management and Disposition
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Cardiac tamponade should be suspected in patients at risk with shock. Point-of-care cardiac ultrasound (POCUS) provides rapid identification of tamponade physiology and should prompt pericardiocentesis if the patient is in shock. Electrocardiogram (ECG), chest x-ray, complete blood count (CBC), and cardiac injury markers are less specific clues for tamponade but are helpful for the identification of other causes of shock. CT of chest will identify cardiac tamponade but will take longer than POCUS to obtain.
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Electrical alternans seen on a 12-lead ECG suggests pericardial effusion.
Cardiac tamponade may cause a narrow pulse pressure, pulsus paradoxus (fall of > 10 mm Hg in systolic blood pressure during inspiration), and low-voltage ECG.
Rapid ultrasonographic identification of pericardial fluid in patients with penetrating chest trauma may lead to lifesaving pericardiocentesis or thoracotomy.
Cardiac tamponade is a treatable cause of PEA.
Beck’s triad of acute cardiac tamponade includes JVD from an elevated central venous pressure, hypotension, and muffled heart sounds but is present only 10% to 40% of the time.
JVD in tamponade may not be seen in hypovolemic states such as trauma.
The simultaneous appearance of all three physical signs of Beck’s triad is a late manifestation of tamponade and usually seen just prior to cardiac arrest.
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